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APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models

ABSTRACT: APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models

PROVIDER: PRJNA1071059 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27785100.fastq.gz	Fastqsanger.gz
	SRR27785101.fastq.gz	Fastqsanger.gz
	SRR27785102.fastq.gz	Fastqsanger.gz
	SRR27785103.fastq.gz	Fastqsanger.gz
	SRR27783448_1.fastq.gz	Fastqsanger.gz

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APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models [fibroblasts]

Project description:Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most frequent cause of dementia. The disease has a substantial genetic component comprising both highly penetrant familial mutations (APP, PSEN1 and PSEN2) and sporadic cases with complex genetic etiology. Mutations in APP and PSEN1/2 alter the proteolytic processing of APP to its metabolites, including Ab and APP Intracellular Domain (AICD). In this study, we use transgenic porcine models carrying the human APPsw and PSEN1M146I transgenes to demonstrate the pathobiological relevance of transcriptional regulation facilitated by APP and its AICD domain. Through molecular characterization of hippocampal tissue, we describe the differential expression of gene sets that cluster in molecular pathways with translational relevance to AD. We further identify phosphorylated and unphosphorylated AICD in differential complexes with proteins implicated in signal transduction and transcriptional regulation. Integrative genomic analysis of transcriptional changes in somatic cell cultures derived from pigs treated with g-secretase inhibitor demonstrates the importance of g-secretase APP processing in transcriptional regulation. Collectively, our data supports a model in which APP, and in particular its AICD domain, modulates gene networks associated with AD pathobiology through interaction with signaling proteins.

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APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models [hippocampus]

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APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models [hippocampus]

Project description:APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models [hippocampus]

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APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models [fibroblasts]

Project description:APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models [fibroblasts]

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APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models

Project description:This SuperSeries is composed of the SubSeries listed below.

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miRNA sequencing of exosomes derived from N2A and APP-N2A cells

Project description:APP misexpression plays a crucial role in triggering a complex pathological cascade, leading to Alzheimer’s disease (AD). The aim of this study is for determine the influence of APP ectopic expression on the miRNA profiles of neuronal exosomes. In study, miRNA sequencing was done using the exosomes derived from N2A (control) and APP-N2A (N2A with APP overexpression).

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Project description:The amyloidogenic processing of APP to A-beta is known to play a central role in Alzheimer’s disease pathogenesis. Despite this, however, the physiological role of APP and its processing still remains elusive. In the current study we utilzed a transcriptional profiling approach, to determine the pathways that may become dysregulated in the brains of APPswe transgenic mice (Tg2576). As many pathways linked to Alzheimer’s disease are also linked to cholesterol metabolism, we also treated the Tg2576 mice with LXR agonist TO901317, to determine the effects of LXR agonists on the hippocampal transcriptome of Tg2576 mice. We used microarrays to identify gene expression modulated in hippocampus of transgenic TG2576 mice that express human APP containing the Swedish mutation and the transcriptional responses to treatment with an LXR agonist.

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Project description:Alzheimer’s disease (AD) is a common form of dementia characterized by amyloid plaque deposition, TAU pathology, neuroinflammation and neurodegeneration. Mouse models recapitulate some key features of AD. For instance, the B6.APP/PS1 model (carrying human transgenes for mutant forms of APP and PSEN1) shows plaque deposition and associated neuroinflammatory responses involving both astrocytes and microglia beginning around 6 months of age. However, in our colony, TAU pathology, significant neurodegeneration and cognitive decline are not apparent in this model even at older ages. Therefore, this model is ideal for studying neuroinflammatory responses to amyloid deposition. Here, RNA sequencing of brain and retinal tissue, generalized linear modeling (GLM), functional annotation followed by validation by immunofluorescence (IF) was performed in B6.APP/PS1 mice to determine the earliest molecular changes prior to and around the onset of plaque deposition (2-6 months of age).

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